ObjectiveTo investigate the possible mechanism of Jishe Qushi Capsule （脊蛇祛湿胶囊， JQC） in treating rheumatoid arthritis （RA） from the perspective of macrophage polarization mediated by neutrophil extracellular traps （NETs）. MethodsTwenty-four female SD rats were randomly divided into four groups， blank control group， model group， JQC group， and peptidylarginine deiminase 4 （PAD4） inhibitor group with 6 rats in each group. All groups but the blank control group were subjected to the induction of collagen-induced arthritis （CIA）. After successful model establishment， rats in the JQC group received intragastric administration of JQC 1.47 g/kg daily； rats in the PAD4 inhibitor group received intraperitoneal injections of the PAD4 inhibitor 4 mg/kg weekly. Rats in the blank， model， and PAD4 inhibitor groups received 2 ml of pure water daily by gavage. All treatments lasted 4 weeks. Joint lesions of each group were assessed on day 7， 14， 21， 28， and 35 after model establishment， and arthritis index （AI） scores were recorded. At 24 h after the final administration， histopathology of knee joints， including HE staining， safranin O-fast green staining， and TRAP staining， was performed. Flow cytometry was used to detect the counts of M1 and M2 macrophages in peripheral blood. ELISA was used to determine serum levels of TRACP， NETs， TNF-α， IL-1β， and iNOS. Western Blotting and qRT-PCR were used to measure MPO， NE， RANKL， OPG， and p65 protein and mRNA expression in knee cartilage tissue. ResultsCompared with the blank control group， the model group showed increased AI scores （P＜0.05）， marked synovial inflammatory infiltration， angiogenesis， and bone-cartilage destruction， increased TRAP-positive osteoclasts， increased M1 macrophages and decreased M2 macrophages， elevated serum TRACP， NETs， TNF-α， IL-1β， and iNOS （P＜0.05）， elevated MPO， NE， RANKL， and p65 protein/mRNA expression and decreased OPG protein/mRNA expression in knee cartilage tissue （P＜0.05）. Compared with the model group， the JQC group exhibited improved synovial inflammation， angiogenesis， and bone-cartilage damage， reduced AI scores on day 21， 28， and 35， decreased osteoclast counts， decreased M1 macrophages and increased M2 macrophages， reduced serum TRACP， NETs， TNF-α， IL-1β， and iNOS （P＜0.05）， decreased MPO， NE， RANKL， and p65 protein/mRNA expression and increased OPG expression （P＜0.05）. Compared with the PAD4 inhibitor group， the JQC group showed significantly lower AI scores， reduced M1 macrophages， increased M2 macrophages （P＜0.05）， reduced serum TRACP， TNF-α， IL-1β， and iNOS， decreased MPO， RANKL， and p65 expression， and increased OPG levels （P＜0.05）. ConclusionThe therapeutic mechanism of JQC for RA may involve inhibition of NETs formation， downregulation of the RANKL/NF-κB signaling pathway， and regulation of macrophage M1/M2 polarization imbalance， thereby suppressing osteoclastogenesis and inflammatory bone destruction.

Objective:To investigate the utilization of Internet plus nursing service and its influencing factors.Methods:From October 2018 to January 2019, 247 patients registered on the Internet plus nursing service platform were randomly surveyed to understand the status quo of Internet plus nursing service. The influencing factors were analyzed based on the Anderson health service model.Results:Among the 247 patients who received Internet plus nursing, 74.5%(184 cases) were women. The average age was 37 years(20-81 years). The median number of times of nursing service received by the patients was 2 times. Infusion was the most accepted nursing service on the platform. Patients who are older, do not have basic medical insurance, the source of routine care is not a Class A tertiary hospital, and do not have chronic diseases used the Internet platform to receive nursing services more frequently.Conclusions:Internet plus nursing service has been initially recognized by patients. The predisposing factor affecting the tendency of individuals to continue using Internet plus nursing services is age, enabling factors are health insurance status and regular nursing sources, and the need factor is chronic disease.

Objective To investigate the effect of PM2.5 airborne particulate matter with a mean diameter of less than 2.5μm exposure on autophagy and explore the links between autophagy and apoptosis in human lung cancer cells(A549). Methods A549 cells were exposed to 100μg/mL PM2.5 with or without 3-MA(autophagy inhibitor)for various periods of 0、2、4、12 or 24 hrs. Autophagy in A549 cells was assessed by determining the lev-el of LC3(a known autophagy marker)using confocal microscopy. The level of microtubule-associated protein 1 light chain 3(LC3) Ⅱ conversion and Bax (a pro-apoptotic protein) was detected by western blotting. Results The expression of LC3 and the ratio of LC3-II/LC3-I in A549 cells was significantly increased and Bax was signifi-cantly decreased following exposure to PM2.5100 μg/mL for 24 h in a time-dependent manner(P < 0.05). After treated with 100 μg/mL PM2.5,the formation of LC3 in A549 cells as evidenced by the intensity of intracellular fluorescence was significantly increased ,and autophageosomes were observed around nucleus in A549 cells. Fur-thermore blockage of autophagy by 3-MA led to a significant increase in the pro-apoptotic protein Bax. Conclu-sion PM2.5 exposure induces autophagy which may protect against apoptosis induced by PM2.5 in A549 cells.

Lots of evidence show a correlation between air pollution and chronic respiratory diseases, of which the effect of particulate matter is the most concerned.It is the current research hotspot that respiratory diseases in both children and adults are closely related with atmospheric pollution levels.The influence mechanisms of atmos-pheric pollution on respiratory diseases include oxidative stress, inflammation, genetic damage, etc.This paper made a review of the latest advances s on the pathogenesis of chronic respiratory diseases caused by atmospheric particulates PM2.5 .